The aim of these studies is a genetic analysis of rDNA magnification and rDNA stability in Drosophila melanogaster. rDNA magnification occurs in Drosophila males carrying an aberrant Y chromosome and results in a high frequency of heritable, but sometimes unstable changes in rDNA redundancy. My first objective is to isolate and characterize a number of magnification-defective mutations and to further analyse one such mutation (mei-41) which I have previously identified. In addition to their value in the analysis of the magnification process itself, the study of these mutations will also determine if they are defective in the normal maintenance of rDNA (as is mei-41) in other processes of gene amplification, or in general processes such as recombination and repair. Secondly, I propose to map and characterize the mutation on the Y chromosome which induces rDNA magnification in order to determine the wild-type function of this gene or site. My third goal is to determine which if any heterochromatic sites or regions on the X chromosome are required for magnification. Lastly, I argue that in terms of biological significance, magnification might be thought of as an aberrant expression of a redundancy control mechanism normally possessed by Drosophila or as a transposon-mediated phenomena similar to hybrid dysgenesis. I propose to test the first hypothesis by using a bacterial exotoxin, whose toxicity to flies is a metric of the number of functional rRNA genes they possess, to select for rDNA increases in wild-type populations and to determine if they have arisen by magnification or by a magnification-like mechanism. To test the relevance of a transposon-mediated mechanism, I intend to look for a magnification-associated mutator activity and, if I find it, to determine if the induced mutations are a consequence of insertion of material from the rDNA. I also propose to study the instability of some magnified rDNA loci in terms of transposon-mediated breakage or recombination events. These experiments are relevant to the overall problem of the control of gene redundancy and to the question of how genome structure is faithfully maintained.